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Calcium Metabolism & Related Diseases

Calcium Metabolism & Related Diseases. Objectives. Calcium functions & metabolism Vitamin D functions & metabolism Calcium homeostasis Vitamin D Parathyroid Hormone (PTH) Calcitonin Hormone Rickets & Osteomalacia Hypocalcaemia & hypercalcaemia Osteoprosis. Components of BONEs.

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Calcium Metabolism & Related Diseases

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  1. Calcium Metabolism & Related Diseases

  2. Objectives • Calcium functions & metabolism • Vitamin D functions & metabolism • Calcium homeostasis • Vitamin D • Parathyroid Hormone (PTH) • Calcitonin Hormone • Rickets & Osteomalacia • Hypocalcaemia & hypercalcaemia • Osteoprosis

  3. Components of BONEs Bone is a specialized mineralized connective tissue containing: 1- Cellular Elements: - Osteoblasts (bone forming cells) - Osteoclasts (bone resorpting cells) 2- Organic Matrix - Proteins: Type I Collagen Proteoglycan - Inorganic Minerals: Calcium & Phosphate - Others: small amount of hydroxide and carbonate • Calcium is tightly regulated with phosphorous in the body

  4. CALCIUM • Calcium is the most abundant mineral in the body: • ~ 1 kg in a 70 kg man • ~ 99% of the body’s calcium is present in the bone where it is combined with phosphate

  5. Biological function of calcium • Bone formation • 99 % • in bone • Reservoir for ECF [Ca2+] • Clotting Total Calcium • ECF • Excitability of nerve & muscle • 1 % • Metabolic regulation for action of hormones & enzyme activation • ICF

  6. Calcium homeostasis

  7. Sources of calcium • Excellent: Milk, milk products as cheese & yoghurt • Fair Legumes, vegetables

  8. Calcium in Blood

  9. Calcium homeostasis • Parathyroid Hormone (PTH) • Active Vitamin D (1,25 DHCC) • Calcitonin Hormone Plasma [Ca2+] is regulated by:

  10. Vitamin D A group of sterols with a hormone-like function. Sources of Vitamin D 1- Skin synthesis (On Exposure to Sun Lights): In the skin, 7 dehydrocholesterol is converted to vitamin D3 by exposure to sunlight 2- Diet: - Animal Source Cholecalciferol (Vitamins D3) - Plant Source: Ergocalciferol (Vitamin D2) Vitamin 2 & D3 are NOTbiologically active Activation of cholecalciferol(vitamin D3) Cholecalciferol (Vitamin D3) is activated in vivo to the biologically active form by two hydroxylations: first in the liver (at position 25) by 25 hydroxylase & then in the kidney at positions 1 by 1 α hydroxylase Active Vitamin D 1, 25 dihydroxycholecalciferol (Calcitriol )

  11. SOURCES OF VITAMIN D Vitamin D2 plant source DIET VITAMINs D Vitamin D3 animal source fatty fish Liver egg yolk Sun Rays 7-dehydrocholesterol In the skin

  12. Vitamin D metabolism • Cholecalciferol (Vitamin D3) is derived from 7-dehydrocholesterol in the skin by sunlight or supplied in the diet • In liver: Cholecalciferol is converted to 25-hydroxycholecalciferol (25-HCC) by the enzyme 25 hydroxylase • 25-hydroxycholecalciferol is the predominant form of vitamin D in blood • 25-hydroxycholecalciferol is the main storage form of vitamin in the body • In kidneys: The 1 α hydroxylase enzyme converts 25-hydroxycholecalciferol to 1,25-dihydroxycholecalciferol (1, 25 DHCC) which is biologicallyactive form of vitamin D

  13. Vitamin D functions Active vitamin D (1, 25 DHCC) regulates calcium levels in the body (calcium homeostasis) Through: • Increasing absorption of calcium by the intestine • Minimizing loss of calcium by kidney • Stimulating resorption of bone when necessary Deficiency of Active Vitamin D (1: 25-DHCC) Defective Bone Mineralization (calcification)

  14. Vitamin D functions

  15. Osteomalacia & Rickets Rickets & osteomalacia are bone diseases occurring due to poor mineralization (calcium content) of bone Causes I. Vitamin D deficiency 1- Deficiency of sources of vitamin D3: BOTH: Nutrional Vitamin D deficiency Poor exposure to sun light 2- Impaired vitamin D metabolism: Renal Rickets: deficiency of 1 hydroxylase of the kidney Deficiency of parathyroid hormone : decrease activity of 1 α hydroxylase II. Calcium deficiency

  16. Vitamin D deficiency calcium of bone is mobilized outside bone with demineralizationof bone Rickets Osteomalacia (in children) (in adults)

  17. Renal Rickets (Renal osteodystrophy) Chronic Renal Failure Low activity of renal 1a-hydroxylase Decreased ability to form the active form of vitamin D (1, 25 DHCC) Treatment: 1,25 DHCC (Calcitriol)

  18. RICKETS Normal formation of the collagen matrix BUT incomplete mineralization (poor calcification) softbones (like rubber) Bone Deformity ------------------------------------------------------------------------------------ OSTEOMALACIA demineralization (poor calcification) of preexisting bones with More Susceptibility toFracture

  19. Laboratory Diagnosis of Osteomalacia & Rickets due to Vitamin D deficiency •  Blood levels of 25-hydroxycholecalciferol (25 HCC) • Blood calcium (hypocalcemia) •  Blood Alkaline phosphatase

  20. Parathyroid hormone (PTH) PTH is the principal acute regulator of plasma [Ca2+]

  21. Parathyroid Hormone (PTH) • The active hormone is secreted in response to al fall in plasma Ca2+ resulting in in Ca2+ increase in blood. • On bone: PTH stimulates bone resorption by osteoclasts resulting in release of calcium ions from bones to blood in cases of hypocalcemia • On kidney: 1- PTH increases reabsorption of calcium from kidney tubules. 2- PTH promotes activity of 1a hydroxylase of the kidney (with more hydroxylation of 25 hydroxycholecalciferol (25 HCC) to 1,25 DHCC (activation of vitamin D) which increases intestinal absorption of calcium So, action of PTH on intestine is indirect (via Vitamin D)

  22. Parathyroid Hormone (PTH)

  23. Calcitonin Hormone Calcitonin hormone : • secreted by the parafollicular or “C” cells of the thyroid gland • Released in response to high blood calcium (hypercalcemia) In cases of hypercalcemia, Calcitonin Hormone  blood [Ca2+] by: • Osteoclast activity (preventing release of calcium to blood) • Renal reabsorption of calcium Net result of its action  blood calcium CALCITONIN IS THE ONLY HYPOCALCEMIC HORMONE

  24. MAIN CAUSES of Hypocalcaemia • Hypoparathyroidism ( PTH) • Vitamin D deficiency • Renal disease (low 1 a hydroxylase) • Hypoprotenemia ( Plasma Proteins) • Nutritional calcium deficiency

  25. MAIN CAUSES of Hypercalcaemia • Hyperparathyroidism • Malignant disease • Drugs as lithium • Thyrotoxicosis

  26. Osteoporosis • Reduction in bone mass per unit volume • Bone matrix composition is normal but it is reduced • Post-menopausal women lose more bone mass than men (primary osteoporosis)

  27. Osteoporosis Secondary osteoporosis may be caused by: • Drugs • Immobilization • Smoking • Alcohol • Cushing’s syndrome • Hyperthyroidism

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